A patient with benign prostatic hyperplasia has increased post-void residual volume, indicative of bladder outlet obstruction. Which of the following best explains the pathophysiological mechanism behind this obstruction?
Group of answer choices
- Reduced testosterone levels leading to prostatic tissue scarring
- Increased smooth muscle relaxation in the bladder neck
- Increased cortisol levels causing prostate tissue shrinkage
- Hyperplasia and hypertrophy of prostatic tissue leading to urethral compression
The correct answer is:
Hyperplasia and hypertrophy of prostatic tissue leading to urethral compression
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Explanation:
Benign prostatic hyperplasia (BPH) causes bladder outlet obstruction primarily due to:
- Hyperplasia (↑ cell number) and hypertrophy (↑ cell size) of prostatic stromal and epithelial cells in the transition zone of the prostate.
- This enlarges the prostate, compressing the prostatic urethra, leading to:
- Increased post-void residual volume (incomplete bladder emptying).
- Obstructive symptoms (weak stream, hesitancy, urinary retention).
Why Not the Others?
- Reduced testosterone levels causing scarring: BPH is not caused by low testosterone; it’s linked to dihydrotestosterone (DHT) stimulation of prostate growth.
- Increased smooth muscle relaxation in the bladder neck: BPH involves increased smooth muscle tone (α1-adrenergic mediated), not relaxation.
- Increased cortisol causing prostate shrinkage: Cortisol does not shrink the prostate; BPH is driven by androgens (DHT) and aging.
Key Pathophysiology:
- DHT (derived from testosterone via 5α-reductase) promotes prostate growth.
- α1-adrenergic receptors in the prostate increase smooth muscle tone, worsening obstruction.
Thus, prostatic tissue hyperplasia/hypertrophy is the core mechanism.
